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New Drugs Regulating Cytoskeletons in Human Health and Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 1666

Special Issue Editors


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Guest Editor
Institute of Neurophysiopathology, CNRS UMR7051, Aix-Marseille University, Marseille, France
Interests: the role of the microtubule-associated protein Tau; the impact of new chemotherapeutic molecules

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Guest Editor
Mediterranean Institute of Biodiversity and Marine and Continental Ecology (IMBE), CNRS UMR7263, IRD237, Aix-Marseille University, Marseille, France
Interests: medicinal chemistry

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Guest Editor
Institute of Neurophysiopathology, CNRS UMR7051, Aix-Marseille University, Marseille, France
Interests: cytoskeleton

Special Issue Information

Dear Colleagues,

It is a great pleasure to invite you to contribute to the Special Issue entitled “New drugs regulating cytoskeletons in human health and diseases”. The cytoskeletons constitute so many functional networks involved in biological processes, such as cell division and mechanotransduction, motility, intracellular organelles trafficking and macromolecules, and cell morphogenesis. Given that they are a key component of eukaryotic cells, it is not surprising that they continue to represent a prime pharmacological target in human health and diseases.

Exploratory research is being conducted in many laboratories around the world, and both synthetic and natural compounds or their derivatives with therapeutic properties are being investigated. Non-primary use of known drugs is also under research.

This Special Issue welcomes original articles and reviews addressing the search for new agents and the repurposing of known drugs for the treatment of cytoskeleton-associated diseases.

Dr. Gilles Breuzard
Dr. Maxime Robin
Dr. Hervé Kovacic
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • tubulin
  • actine
  • cytoskeletons
  • associated proteins
  • pharmacological agent
  • repurposing of drugs
  • oncology
  • neurodegenerative diseases

Published Papers (2 papers)

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Research

19 pages, 3969 KiB  
Article
Roles of Thermosensitive Transient Receptor Channels TRPV1 and TRPM8 in Paclitaxel-Induced Peripheral Neuropathic Pain
by Wen-Wen Li, Yan Zhao, Huai-Cun Liu, Jiao Liu, Sun-On Chan, Yi-Fei Zhong, Tang-Yu Zhang, Yu Liu, Wei Zhang, Yu-Qi Xia, Xiao-Chun Chi, Jian Xu, Yun Wang and Jun Wang
Int. J. Mol. Sci. 2024, 25(11), 5813; https://doi.org/10.3390/ijms25115813 - 27 May 2024
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Abstract
Paclitaxel, a microtubule-stabilizing chemotherapy drug, can cause severe paclitaxel-induced peripheral neuropathic pain (PIPNP). The roles of transient receptor potential (TRP) ion channel vanilloid 1 (TRPV1, a nociceptor and heat sensor) and melastatin 8 (TRPM8, a cold sensor) in PIPNP remain controversial. In this [...] Read more.
Paclitaxel, a microtubule-stabilizing chemotherapy drug, can cause severe paclitaxel-induced peripheral neuropathic pain (PIPNP). The roles of transient receptor potential (TRP) ion channel vanilloid 1 (TRPV1, a nociceptor and heat sensor) and melastatin 8 (TRPM8, a cold sensor) in PIPNP remain controversial. In this study, Western blotting, immunofluorescence staining, and calcium imaging revealed that the expression and functional activity of TRPV1 were upregulated in rat dorsal root ganglion (DRG) neurons in PIPNP. Behavioral assessments using the von Frey and brush tests demonstrated that mechanical hyperalgesia in PIPNP was significantly inhibited by intraperitoneal or intrathecal administration of the TRPV1 antagonist capsazepine, indicating that TRPV1 played a key role in PIPNP. Conversely, the expression of TRPM8 protein decreased and its channel activity was reduced in DRG neurons. Furthermore, activation of TRPM8 via topical application of menthol or intrathecal injection of WS-12 attenuated the mechanical pain. Mechanistically, the TRPV1 activity triggered by capsaicin (a TRPV1 agonist) was reduced after menthol application in cultured DRG neurons, especially in the paclitaxel-treated group. These findings showed that upregulation of TRPV1 and inhibition of TRPM8 are involved in the generation of PIPNP, and they suggested that inhibition of TRPV1 function in DRG neurons via activation of TRPM8 might underlie the analgesic effects of menthol. Full article
(This article belongs to the Special Issue New Drugs Regulating Cytoskeletons in Human Health and Diseases)
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18 pages, 6907 KiB  
Article
Imbalance between Actin Isoforms Contributes to Tumour Progression in Taxol-Resistant Triple-Negative Breast Cancer Cells
by Vera Dugina, Maria Vasileva, Natalia Khromova, Svetlana Vinokurova, Galina Shagieva, Ekaterina Mikheeva, Aigul Galembikova, Pavel Dunaev, Dmitry Kudlay, Sergei Boichuk and Pavel Kopnin
Int. J. Mol. Sci. 2024, 25(8), 4530; https://doi.org/10.3390/ijms25084530 - 20 Apr 2024
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Abstract
The widespread occurrence of breast cancer and its propensity to develop drug resistance highlight the need for a comprehensive understanding of the molecular mechanisms involved. This study investigates the intricate pathways associated with secondary resistance to taxol in triple-negative breast cancer (TNBC) cells, [...] Read more.
The widespread occurrence of breast cancer and its propensity to develop drug resistance highlight the need for a comprehensive understanding of the molecular mechanisms involved. This study investigates the intricate pathways associated with secondary resistance to taxol in triple-negative breast cancer (TNBC) cells, with a particular focus on the changes observed in the cytoplasmic actin isoforms. By studying a taxol-resistant TNBC cell line, we revealed a shift between actin isoforms towards γ-actin predominance, accompanied by increased motility and invasive properties. This was associated with altered tubulin isotype expression and reorganisation of the microtubule system. In addition, we have shown that taxol-resistant TNBC cells underwent epithelial-to-mesenchymal transition (EMT), as evidenced by Twist1-mediated downregulation of E-cadherin expression and increased nuclear translocation of β-catenin. The RNA profiling analysis revealed that taxol-resistant cells exhibited significantly increased positive regulation of cell migration, hormone response, cell–substrate adhesion, and actin filament-based processes compared with naïve TNBC cells. Notably, taxol-resistant cells exhibited a reduced proliferation rate, which was associated with an increased invasiveness in vitro and in vivo, revealing a complex interplay between proliferative and metastatic potential. This study suggests that prolonged exposure to taxol and acquisition of taxol resistance may lead to pro-metastatic changes in the TNBC cell line. Full article
(This article belongs to the Special Issue New Drugs Regulating Cytoskeletons in Human Health and Diseases)
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